The investigators propose to evaluate whether changes in cytoskeleton play a role in or are simply a consequence of programmed cell death. The investigators have established that collapse of the actin cytoskeleton is one of the earliest events of the spontaneous death of salivary gland cells during metamorphosis of Drosophila; a few other researchers have likewise identified early changes in the cytoskeleton of cells undergoing apoptosis. These changes have been associated with blebs in the cell membrane at late apoptosis or cytoskeletal proteins have been examined as targets for caspases or other proteases, leading to the hypothesis that collapse of the cytoskeleton is a late consequence. The investigators hypothesize that disruption of intracellular trafficking, by direct action on cytoskeletal proteins, is an early rather than a late component of apoptosis. The investigators will establish a chronological sequence of specific events in this model of apoptosis. The investigators will correlate the status of the actin and tubulin cytoskeleton during early and late apoptosis (evaluated by fluorescence microscopy and western blotting) with changes in metabolic activity (respiration, lysosomal movement), macromolecular expression (by examination of alteration in protein synthesis), and activation of Drosophila caspases (evaluated by identification of proteolytic fragments, measurement of enzymatic activity, and use of inhibitors). The investigators will establish a model in which the death of the salivary gland can be completely controlled in vitro so that the investigators evaluate causal relationships by directly controlling several parameters. The investigators will attempt to stabilize and disrupt the cytoskeleton as the glands involute in vitro, and observe the effect on the progress of apoptosis, and likewise inhibit proteolysis and mRNA and protein synthesis, and observe the impact on cytoskeleton and cell death. These studies will contribute to our understanding of the means by which a cell commits itself to die, and will provide information that can be further used to evaluate the specific signaling pathway that regulates the onset and the profession of cell death. These findings will be valuable for the development of therapeutic approaches so that we can manipulate the pattern of cell death in gerontology, oncology, neurology, and immunology.